Saturday, May 7, 2016

How Did Birds Get Their Wings? Bacteria May Provide a Clue to the Genomic Basis of Evolutionary Innovation, Say Evolutionists

30 Days of Evolution

That evolution occurred is known to be a fact but how evolution occurred is not known. In particular we are ignorant of how evolutionary innovations arose. Of course biological novelties and innovations arose from a series of random chance events, but it is less than reassuring that we cannot provide more detail. How exactly did the most complex designs spontaneously arise? What mechanisms overcame, over and over, the astronomical entropy barriers, by sheer luck of the draw? As Craig MacLean’s and Andreas Wagner’s, and coworker’s, new PLOS Geneticspaper begins, “Novel traits play a key role in evolution, but their origins remain poorly understood.” Could it be that evolution is not actually a fact? No, not according to evolutionists. And this new paper claims to provide the basis for how the seemingly impossible became the mundane.

The paper begins by summarizing the many proposed genetic mechanisms for the evolution of biological innovations:

An evolutionary innovation is a new trait that allows organisms to exploit new ecological opportunities. Some popular examples of innovations include flight, flowers or tetrapod limbs [1,2]. Innovation has been proposed to arise through a wide variety of genetic mechanisms, including: domain shuffling [3], changes in regulation of gene expression [4], gene duplication and subsequent neofunctionalization [5,6], horizontal gene transfer [7,8] or gene fusion [9]. Although innovation is usually phenotypically conspicuous, the underlying genetic basis of innovation is often difficult to discern, because the genetic signature of evolutionary innovation erodes as populations and species diverge through time.

The unspoken problem here is, as usual, serendipity. The various proposed genetic mechanisms for the evolution of biological innovations all suggest an amazing bit of fortuitous luck. For random chance events just happened to create these various complicated structures and mechanisms (such as horizontal gene transfer and protein domains their shuffling) which then produced new evolutionary breakthroughs.

Evolution didn’t know what was coming. Evolution did not plan this out, it did not realize that horizontal gene transfer would lead the way to new biological worlds. The evolution of horizontal gene transfer would require a long sequence of random mutations, many of which would not provide any fitness advantage. And when the construction project was completed, and the first horizontal gene transfer capability was possible, there would be no immediate advantage.

This is because there would have been no genes to transfer. The mechanism works only when it is present in more than one, neighboring, cells. One cell gives, and another cells receives. By definition the mechanism involves multiple cells.

But it doesn’t stop there. Even if the first horizontal gene transfer capability was able to spread across a population, and even if it did provide a fitness advantage to the fortunate citizens, there would not be even a hint of the enormous world of biological innovations that had just been opened.

In other words, what this evolutionary narrative entails is monumental serendipity. Biological structures and mechanisms (horizontal gene transfer in this case, but it is the same story with the other hypotheses listed above) are supposed to have evolved as a consequence of a local, proximate, fitness advantage: a bacteria could now have a gene it didn’t have before.

But it just so happened that the new structures and mechanisms would also, as a free bonus, be just what was needed to produce all manner of biological innovations, far beyond assisting a lowly bacteria increase its fecundity.

This is monumental serendipity.

The science contradicts the theory

Undaunted, the new paper finds that one of the other mechanisms, gene duplication and subsequent neofunctionalization, is a key enabler and pathway to biological innovations.

That conclusion resulted from what otherwise was a fine piece of research work. The experimenters exposed different populations of Pseudomonas aeruginosa, a dangerous infectious bacteria, to 95 new sources of its favorite food: carbon.

The bacteria had to adjust to the new flavors of carbon and they did so with various genetic modifications, including various genetic mutations. In the most challenging cases (where the new carbon sources were most difficult for the bacteria to adjust to), the bacteria often produced mutations in genes involved in transcription and metabolism. And these mutations often occurred in genes where there were multiple copies, so the mutations occurred in one copy while the other copy could continue in its normal duties.

The problem is, these genetic duplicates were preexisting in the P. aeruginosa genome. This is yet another instance of serendipity.

Why? Because preexisting duplicates are not common. Only about 10% of the genes have duplicates lying around, and fortunately, the genes needed for adaptation (involving transcription and metabolism) just happened to have such duplicates.

Now there were a few instances of de novo gene duplication. That is, once the experiment began, and after the P. aeruginosa populations were exposed to the challenging diets, a total of six genes underwent duplication events. But in each and every case, the duplication events occurred repeatedly and independently, in different populations (for each of the 95 different carbon sources, the experimenters ran four parallel trials with independent populations).

This result indicates directed gene duplication. This is because it is highly unlikely that random, chance, gene duplication events just happened hit on the same gene in different populations. Here is an example calculation.

Let’s assume that in the course of the experiment, which ran for 30 days and about 140 generations of P. aeruginosa, some genes may undergo duplication events by chance. Next assume there is a particular gene that needs to be duplicated and modified in order to for P. aeruginosa to adapt to the new food source. (Note that there may be several such genes, but as we shall see that will not affect the conclusion). Given that there are four separate, independent trials, what is the probability that the gene will be duplicated in two or more of those trials?

Let P_dup be the probability that any gene is duplicated in the course of the experiment. For our gene of interest, it may be duplicated in 0, 1, 2, 3, or all 4 of the trials. The binomial distribution describes the probability, P, of each of these outcomes. To answer our question (i.e., What is the probability that the gene will be duplicated in two or more of those trials?) we sum the binomial distribution’s value for N = 2, 3 and 4. In other words, we calculate P(2) + P(3) + P(4).

This will give us the probability of observing what was observed in the experiment (i.e., the duplication events occurred repeatedly and independently, in different populations, in all 6 cases where duplication events were observed).

Well for a reasonable value of P_dup, the probability that any gene is duplicated in the course of the experiment, such as 0.0001, the probability of observing multiple duplications events for any given food source (i.e., P(2) + P(3) + P(4)) is about 60 in one billion, or 6 times 10^-8. Even worse, the probability of observing this in all 6 cases where duplication events were observed is about 5 times 10^-44.

It isn’t going to happen.

Exceptionally high rates of gene duplication, in particular genomic regions of Salmonella typhimurium, in a high growth rate medium, were observed to be about 0.001 and even slightly above 0.01 in rare cases.

If we go all out and set P_dup to an unrealistically high 0.1, our results are still unlikely. The P(2) + P(3) + P(4)) is .05, and the probability of observing this in all 6 cases where duplication events were observed is about 2 times 10^-8.

In order to raise these probabilities to reasonable levels, such that what was observed in the experiment is actually likely to have occurred, we need to raise P_dup to much higher values. For example, for a P_dup of .67 (two-thirds probability), P(2) + P(3) + P(4)) is .89, and the probability of observing this in all 6 cases where duplication events were observed is about .5.

But even this doesn’t work. For if we were to imagine unrealistically high P_dup values of 0.1 or higher, then massive numbers of duplication events would have been observed in the experiments.

But they weren’t.

Once again, the science contradicts the theory. Our a priori assumption that evolution is a fact, and that the P. aeruginosa adaptations to the new food sources were driven by random mutations, did not work. The theory led to astronomically low probabilities of the observed results.

What the observed gene duplications are consistent with is directed gene duplications. Just as mutations have been found to be directed in cases of environmental challenges, it appears that gene duplications may also be directed.

The paper’s premise, that biological innovations such as flowers and wings are analogous to bacteria adapting to new nutrient sources, is fallacious. But setting that aside, the experimental results do not make sense on evolution’s mechanism of random mutations and natural selection. Instead, the results indicate directed adaptation.

93 comments:

Rapid Evolution of Citrate Utilization by Escherichia coli by Direct Selection Requires citT and dctA. - Feb. 2016The isolation of aerobic citrate-utilizing Escherichia coli (Cit(+)) in long-term evolution experiments (LTEE) has been termed a rare, innovative, presumptive speciation event. We hypothesized that direct selection would rapidly yield the same class of E. coli Cit(+) mutants and follow the same genetic trajectory: potentiation, actualization, and refinement. This hypothesis was tested,,, Potentiation/actualization mutations occurred within as few as 12 generations, and refinement mutations occurred within 100 generations.,,,E. coli cannot use citrate aerobically. Long-term evolution experiments (LTEE) performed by Blount et al. (Z. D. Blount, J. E. Barrick, C. J. Davidson, and R. E. Lenski, Nature 489:513-518, 2012, http://dx.doi.org/10.1038/nature11514 ) found a single aerobic, citrate-utilizing E. coli strain after 33,000 generations (15 years). This was interpreted as a speciation event. Here we show why it probably was not a speciation event. Using similar media, 46 independent citrate-utilizing mutants were isolated in as few as 12 to 100 generations. Genomic DNA sequencing revealed an amplification of the citT and dctA loci and DNA rearrangements to capture a promoter to express CitT, aerobically. These are members of the same class of mutations identified by the LTEE. We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved. http://www.ncbi.nlm.nih.gov/pubmed/26833416

To merely duplicate a gene is not enough. That duplicate requires a binding site or else it is useless. Then that binding site needs to be activated. In Lenski's LTEE the ability to utilize citrate in an aerobic environment was had by duplicating the gene for the citrate transport protein- normally repressed in the presence of O2- and putting it under the control of an existing binding site that was activated in the presence of O2 so that the gene could be expressed.

An existing function utilized in an environment that normally repressed it.

Evos will tell us that chance alone did that- natural selection doesn't help until the deed is done- ie took the only possible gene that could confer some advantage and put it under control of an existing binding site that just happened to allow its expression. And then they'll call it science! Theirs' is no different than magic.

In in eukaryotes it is even more challenging as the binding sites are hundreds to thousands of nucleotides away due to the way the DNA coils around histones.

With prokaryotes gene duplication to an existing binding site is like regular chess whereas with eukaryotes it is more like 3D chess

Or maybe Chubs thinks this experiment was directed by the Great Bacteria God. The GBG heard the cries of his suffering, starving P. aeruginosa believers. The GBG then blessed the poor little guys with the mutations that allowed them to feed on different forms of carbon. Not all got the mutations, and every one who did got different mutations but hey, the GBG works in mysterious ways!

"This revolution has revealed a world as inaccessible to Darwin as outer space was to cavemen. And it has helped to answer the single most important question about evolution, the question that Darwin and generations of scientists after him did not, could not touch: How does nature bring forth the new, the better, the superior? How does life create?You might be puzzled. Wasn’t that exactly Darwin’s great achievement, to understand that life evolved and to explain how? Isn’t that his legacy? Yes and no. Darwin’s theory surely is the most important intellectual achievement of his time, perhaps of all time. But the biggest mystery about evolution eluded his theory. And he couldn’t even get close to solving it." [Wagner, 'Arrival of the fittest' ,ch.1 'What Darwin Didn’t Know']So Darwin's theory is perhaps the "most important intellectual achievement of all time", but could not get even close to solve the question how life evolved or created.If we add that Darwin was also unable to provide a definition of life and had no concept of inheritance, one may wonder what it is that his theory actually explains.

Cornelius Hunter: Exceptionally high rates of gene duplication, in particular genomic regions of Salmonella typhimurium, in a high growth rate medium, were observed to be about 0.001 and even slightly above 0.01 in rare cases.

That's per cell, which means that in a small colony of bacteria, gene duplications of any particular site are virtually inevitable.

"Spontaneous tandem duplications are frequent mutational events throughout the Salmonella chromosome; the frequency of cells carrying a duplication of a particular site ranges from approximately 10^-4 to 3 X 10^-2."

That's per cell, which means that in a small colony of bacteria, gene duplications of any particular site are virtually inevitable.

I think what you are going to need is for duplication events to be strongly deleterious save for the 6 observed duplications (since there were no de novo duplications observed except for those 6). Some fitness loss has been indicated and suggested in the past, but what you are going to need is a big shift away from the typical evolutionary view that gene duplication events are mainly neutral, and an important source of variation (serendipitously, btw, since evolution would have had to create the source).

So it seems that you either have (i) directed, adaptive, duplication events, or (ii) evidence that duplications are much more deleterious than thought.

Cornelius Hunter: I think what you are going to need is for duplication events to be strongly deleterious save for the 6 observed duplications (since there were no de novo duplications observed except for those 6).

Recombination will be about as likely to loss a duplication as to gain a duplication.

Charles darwin:"If it could be demonstrated that any complex organ existed, which could NOT possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down." [Darwin 1859, pg. 175].

Joe G: "Yes, that is ID, CT. You would have known that had you understood what is actually being debated. That you had to ask says that you are trying to debate a topic that you don't understand."

Isn't that the whole point of a blog like this, to try and shed light on something you don't understand? Cornelius used a term in a particular way and I wanted to better understand exactly what he meant from it. Learning is about asking questions.

Zach:If recombination can eliminate a duplication, then they disappear before any beneficial mutations happen. They might even disappear after the good mutations happen. This makes evolution even more unlikely.

natschuster: If recombination can eliminate a duplication, then they disappear before any beneficial mutations happen.

That's right.

natschuster: They might even disappear after the good mutations happen.

It's possible, but less likely. Once a beneficial mutation occurs, it is more likely than not that the percentage of the population which has the mutation will grow. If a mutation then eliminates the trait, then that organism will be at a disadvantage to all the others which still have the beneficial mutation. This process is called natural selection.

Zachriel: Once a beneficial mutation occurs, it is more likely than not that the percentage of the population which has the mutation will grow.

Beneficial is relative and most environments change. That means whatever is beneficial also changes. And beneficial also includes loss of function

If a mutation then eliminates the trait, then that organism will be at a disadvantage to all the others which still have the beneficial mutation. This process is called natural selection.

Natural selection is a process of eliminating the less fit over generations. It is the result of happenstance heritable mutations and fecundity. The mutations have to be happenstance. If they are directed, as the evidence shows, then it isn't NS.

CaroleTim- At least I learned about evolutionism before criticizing it and understanding it is untestable garbage. And I learned about it by reading what its experts had to say. That is why I know more about it than people like you, William and ghostrider.

I did the same for ID- I have read what the experts say.

But anyway who knows what you know. You haven't demonstrated any knowledge of anything.

natschuster: But if they are just as likely to disappear before the mutations can happen, it is a problem.

They have a residence time.

"Spontaneous tandem duplications are frequent mutational events throughout the Salmonella chromosome; the frequency of cells carrying a duplication of a particular site ranges from approximately 10^-4 to 3 X 10^-2."

With a beaker full of bacteria, that means nearly every possible duplication exists somewhere in the population at any one time.

The question we are addressing is not whether duplications are common, but why they don't appear random. The solution suggested is that some duplications disappear, since a good mutation didn't happen. This mechanism makes evolution even less likely, since duplicates can disappear before all the beneficial mutations can happen.

William Speardork proves it is unworthy of being here- Yes WS there are many experts of ID- and they do a better job at defending ID than the alleged experts of evolutionism do trying to defend theirs.

But Joke Gallien is an ID expert. He knows all the standard ID lies and empty non-explanations like "common design" and "designed to evolve" and "design is a mechanism". He's proud to show ID's religious roots by claiming all the evidence supports Biblical created "kinds".

Besides Joke also has memorized all the positive evidence for Intelligent Design of life. It's a null set, didn't require either of his functioning neurons. :D

It's infinitely more sensible to be an ID expert than to be Christophobic closet homosexual atheist who believes that dirt gave birth to life, that the universe poofed itself into existence and hippos evolved from single-cell organisms via mutations.

Why are Darwinists so stupid? Is that a neurological condition? Or are the cretins just a bunch of jackasses pretending to be interested in science while their real motivation is that they have a serious bone to pick with Christianity? What's up with the blatant, in-your-face stupidity?

Yes Joke G certainly is the expert in ID. His brilliant leadership and irrefutable technical points are the main reason ID holds such a prominent position in science labs and classrooms around the world today.

Compared to any evoTARD I am an expert in ID. And from the looks of it I know more about the alleged theory of evolution than they do. There's a bunch of evoTARDs over on TSZ trying to tell me that natural selection doesn't include random, as in happenstance, mutations. They say it is silly for saying ns includes RM even after I quote their experts, textbooks and universities supporting my claim.

And we are still waiting for word of anyone using the unguided evolution paradigm for anything. Lenski has shown that evolutionary processes are very limited and have no chance of producing the diversity of life we observe. Yet evoTARDs cling to him like Timmy's diaper poo clings to him.

And in classrooms they mainly teach BIOLOGY. There isn't any science to teach when it comes to unguided evolution.

The ubiquitous and notorious swill of baboon-brain chatter with the typical fetid breath huffing and puffing, supplies us with sufficient forewarning. Like flashing red lights on a dark foreboding road spelling out, "danger! professional imbeciles at work", we are amply precautioned that Darwinits are infesting the comments section like rabid cockroaches.

I suspect that every time exhaust pipe mouth "ghostrider", posts here the average IQ of the whole blogosphere drops by 10 points. Maybe more.

Indeed, let them hail the great mysterious goddess and the magical god of neo-Darwinism, Lady Luck and Father Time. Oh sorry, I almost left out goddess Sister Slime, the raw materials supplier.

The ubiquitous and notorious swill of baboon-brain chatter with the typical fetid breath huffing and puffing, supplies us with sufficient forewarning. Like flashing red lights on a dark foreboding road spelling out, "danger! professional imbeciles at work", we are amply precautioned that Darwinits are infesting the comments section like rabid cockroaches.

I suspect that every time exhaust pipe mouth "ghostrider", posts here the average IQ of the whole blogosphere drops by 10 points. Maybe more.

Indeed, let them hail the great mysterious goddess and the magical god of neo-Darwinism, Lady Luck and Father Time. Oh sorry, I almost left out goddess Sister Slime, the raw materials supplier.

Calamity:I that hink Dr. Hunter's point was that duplication don't appear to be random. The duplications that turned into beneficial genes occured more often. That means that the duplications are either not random, or most of the other duplications were harmful, and died out.

His point is invalid. They will be duplication events. That's how the genome of bacteria works. Then, some duplications will be deleterious, some neutral, and some beneficial. We will only see the beneficial or neutral ones due to natural selection.

Of course if you decide not to take into account the deleterious events that lead to bacterias dying then it's easy to fool yourself thinking duplication events are not random but directed.

And just think about that : If it's not random, it means the designer as a hand in it. Why would he design new duplications in a experiment made by scientist, with no purpose in the advancement of this bacteria specie ? This does not make sense.

Just spent an hour laughing while reading the foolish rantings of Richard Dawkins in The Selfish Gene. That is one demented individual. And to think that he is the high priest of Darwinism. Fools following fools. Blind leading the blind.

"Evidence shows that the mathematical structure of the "DNA system", is the same as that of the physical universe." Where did you got that ? Any sources ? Or did you got that from some kind of mathematical trance ?

I don't know where you got that either. The tree of life comes from the relationship between living organism due to common descent.

The Tree of Life that I'm talking about comes from a thousand-year old book called Genesis. It essentially means that life (the genome) is organized hierarchically. That was a long, long time before a bunch of clueless dirt worshippers showed up acting like they own the fucking place.

The genome is not stricly and hierarchically organized. It's fucking mess.

Are you willing to put some serious money on this? Or are you just talking out of your asteroid?

Everybody who work on genomic data will tell you that.

No they won't. Google "genome hierarchy" and get some education, goddammit. It's intelligent design all the way. It has always been intelligent design.

Another laughable Darwinist idea under the guise of science. No wonder there is an evolution rethink movement underway. Even Darwinists realize how foolish they look. Go to the following link for a good laugh: